EDITORIAL COPD AND ENVIRONMENT
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Effects of short- and long-term exposures to ambient air pollution on COPD Eric Garshick Affiliations: Pulmonary and Critical Care Medicine Section, Medical Service, VA Boston Healthcare System, Channing Division of Network Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA. Correspondence: Eric Garshick, Pulmonary and Critical Care Medicine Section, VA Boston Healthcare System, 1400 VFW Parkway, West Roxbury, MA 02132, USA. E-mail: [email protected]
@ERSpublications Two papers in the current issue of ERJ address the link between air pollution exposure and COPD http://ow.ly/yEq23 The London fog episode in 1952 was a sentinel event that indicated that short-term exposure to ambient air pollution could adversely influence the health of persons with chronic obstructive pulmonary disease (COPD). A review of autopsy records indicated a doubling of cases with COPD as a major finding compared with other periods [1]. The association between greater levels of ambient air pollution measured in the community and an increase in subsequent short-term COPD-related mortality and hospitalisations has been confirmed by analysis of health related administrative data, including records of hospital admissions and emergency room visits in the USA, Asia and Europe [2–14]. There are considerably fewer studies assessing the impact of short-term air pollution exposure in COPD patients with disease documented by spirometry. Overall, these studies suggest that COPD patients experience a reduction in pulmonary function as a result of short-term exposures [15–20]. Remarkably, the majority of these previous studies included relatively few subjects and with one exception [21] were not designed to assess exacerbation risk. The study that assessed exacerbation risk [21] included former smokers with moderate-to-severe COPD and measured indoor levels of particles with a cut-off aerodynamic diameter of 2.5 mm (PM2.5) and NO2. Higher levels were significantly associated with more symptoms and an increased risk of experiencing an exacerbation, suggesting that measurement of indoor levels of pollutants in persons who spend considerable time indoors (such as those with significant COPD) may be a more relevant measure of exposure than outdoor levels more commonly assessed. The most robust assessment of the effects of ambient air pollution on pulmonary function (but not limited to patients with COPD) included 3262 former and never smokers (some with repeated assessment) from the US Framingham Heart Study in which spirometry data obtained in 1995–2011 were linked to central-site PM2.5, ozone and NO2 [22]. Pollution measured 24–48 h before spirometry and within ranges considered ‘‘moderate’’ by the US Environmental Protection Agency was associated with a significant reduction in forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC). Mean FEV1 and FVC were normal but 20% were defined as having either asthma or COPD based on physician diagnosis, medication use or symptoms. The effects of pollution were not greater in persons with asthma or COPD. The question of whether chronic air pollution exposure can result in the development of COPD is less clear. Previous cross-sectional studies conducted have suggested an association between long-term air pollution exposure, reduced pulmonary function and increased risk of COPD [23–26]. Two large prospective population-based studies from Denmark [6] and metropolitan Vancouver (BC, Canada) [8] did not have Received: June 14 2014
|
Accepted: June 16 2014
Support statement: E. Garshick has received grants from the National Institute of Environmental Health Sciences (R01 ES019853). Conflict of interest: None declared. Copyright ßERS 2014
558
Eur Respir J 2014; 44: 558–561 | DOI: 10.1183/09031936.00108814
COPD AND ENVIRONMENT | E. GARSHICK
access to pulmonary function data and defined new-onset COPD based on hospitalisation records. Significant associations between a first COPD hospitalisation and modelled NO2 [6], and particulate air pollution as measured by black carbon [8] were observed. Further support of a causal relationship is evidence that chronic particulate air pollution exposure results small airway wall remodelling. In a comparison of lungs obtained at autopsy from non-smoking Mexico City (Mexico) residents (high pollution) and Vancouver residents (low pollution) without previous lung disease, small airways had increased amounts of muscle and fibrous tissue, consistent with remodelling [27]. In a rat model, urban air particles also induced the expression of genes involved in airway wall fibrosis [28]. SCHIKOWSKI et al. [29] assess the impact of pollution on the incidence and prevalence of COPD in a longitudinal study in this issue of the European Respiratory Journal. To obtain a large sample size and achieve a common approach to exposure assessment, they analysed subjects who had previously participated in one of four previous European air pollution studies, had pulmonary function assessed longitudinally with two tests available and who lived in areas where the European Study of Cohorts for Air Pollution Effects (ESCAPE) project modelled residential exposure to PM (n53692) and NO2 (n56550) in 2008–2011. COPD was defined based on the NHANES (National Health and Nutrition Examination Survey) defined lower limits of normal for FEV1/FVC (which provided results similar to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) cut-off value of FEV1/FVC ,0.70). Based on data collected in 2008–2011, exposure model derived values included PM2.5, PM10, NO2, oxides of nitrogen (NOx) and measures of traffic volume. NO2 and PM10 were extrapolated retrospectively using historical air pollution records to provide estimates for the follow-up time-point in all studies and the baseline test in three studies, but it was not possible to extrapolate the traffic data. Although not precisely stated, follow-up of the four cohorts ranged from approximately 11 to 15 years, starting in 1985–1999 with follow-up through 2001–2012. The authors used logistic regression to assess the association between COPD prevalence and incidence defined at follow-up by spirometrically defined cut-offs and air pollution exposures defined using the 2008–2011 exposure model linked to home address. Study specific effect estimates were combined in a meta-analysis, and overall effect estimates (other than for coarse PM) were generally positive but not significantly associated with COPD, other than with measures of traffic volume in females and in neversmokers. Results were similar (but weaker) when extrapolated exposures for NO2 and PM10 were used. The authors appropriately note that due to the many non-statistically significant associations reported, it was not possible to determine whether ambient air pollution contributed to the development of COPD. As the authors note, uncertainty in exposure assessment would make it more difficult to detect associations. An acknowledged limitation is the lack of concurrent exposure measurements and details regarding the extent that the address used to assign exposure in each of the analyses remained stable over the follow-up period are not provided. However, there are also other significant limitations. COPD, as defined by the investigators, was relatively uncommon in most of the study population. At follow-up, the mean ages of European Community Respiratory Health Survey and National Survey of Health and Development populations, which together accounted for more than half the study cohort, were only 43 and 53 years old, respectively. Accordingly, these studies contributed relatively few cases since COPD is primarily a disease of older individuals. Part of the Swiss study on Air Pollution and Lung Disease in adults (SAPALDIA) cohort was included in the population analysed by SCHIKOWSKI et al. [29]. A previous analysis of the effect of particulate air pollution in the full SAPALDIA cohort [30] did not define the outcome categorically, but used pulmonary function as a continuous outcome measure, and reported an improvement in FEV1 as PM10 decreased. A similar approach in the current study would likely have increased the power of the study to detect an effect of exposure. This would be an appropriate approach since a subclinical decline in pulmonary function precedes the development of more significant disease defined using a discrete pulmonary function cut point. Finally, persons who reported asthma either at baseline or follow-up were excluded from analysis. This might be appropriate in a younger population since it would be unlikely that these persons would have true COPD at baseline. However, in persons who subsequently develop disease and in the older individuals in the study population there is likely to be overlap with persons meeting diagnostic criteria for COPD since clinical characteristics of asthma and COPD may overlap [31–33]. A sensitivity analysis that included subjects with presumed asthma might provide additional insight. In a second paper in this issue of European Respiratory Journal, DADVAND et al. [34] report on the effects of exposure to NO2 and PM2.5 on inflammatory biomarkers using land-use regression models developed by ESCAPE in 242 patients with well-documented COPD in metropolitan Barcelona in 2004–2006. Although positive associations between air pollution and elevated circulating inflammatory markers have been reported in previous studies including persons without COPD [35–37], such reports have not been consistently positive [38–41]. Since COPD is already characterised by systemic and pulmonary inflammation [42], it is possible that COPD patients may be particularly sensitive to effects of air pollution on promoting systemic inflammation. DADVAND et al. [34] noted positive associations between
DOI: 10.1183/09031936.00108814
559
COPD AND ENVIRONMENT | E. GARSHICK
short-term exposures (5-day lag) to NO2 and an increase in C-reactive protein and fibrinogen, with a suggestive association with other inflammatory biomarkers and a greater effect in former smokers. There was considerably less evidence for an effect of long-term (.1 year) exposures on these biomarkers. The authors did not provide insight into the lack of association with PM2.5 with these biomarkers that they observed. Exposure to ambient NO2 is a measure of exposure to vehicle exhaust, but one would expect PM2.5 levels to reflect these exposures in an urban environment since vehicular sources also contribute to particulate air pollution. The reasons for lack of an association are uncertain, but likely reflect imprecision in modelling daily exposures. Daily exposure in 2004–2006 was extrapolated from 2009 address-specific annual averages obtained from the land-use regression model. Temporal variability was estimated based on variation of daily background in 2004–2006 obtained from local NO2 and PM10 monitors, and the PM10 data were subsequently used to estimate temporal changes in PM2.5. To summarise, although the findings of both papers are limited by imprecision in exposure assessment, the paper by SCHIKOWSKI et al. [29] is consistent with previous literature suggesting that long-term exposure to air pollution may result in the development COPD. The paper by DADVAND et al. [34] is consistent with the effects of recent air pollution exposures on promoting systemic inflammation. Efforts at improving the precision of exposure estimates in the design of future studies will improve the ability to detect meaningful associations between air pollution exposures and COPD risk, and the effects of air pollution on promoting systemic inflammation in patients with COPD.
References 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23
560
Hunt A, Abraham JL, Judson B, et al. Toxicologic and epidemiologic clues from the characterization of the 1952 London smog fine particulate matter in archival autopsy lung tissues. Environ Health Perspect 2003; 111: 1209–1214. Dominici F, Peng RD, Bell ML, et al. Fine particulate air pollution and hospital admission for cardiovascular and respiratory diseases. JAMA 2006; 295: 1127–1134. Atkinson RW, Kang S, Anderson HR, et al. Epidemiological time series studies of PM2.5 and daily mortality and hospital admissions: a systematic review and meta-analysis. Thorax 2014; 69: 660–665. Sunyer J, Schwartz J, Tobias A, et al. Patients with chronic obstructive pulmonary disease are at increased risk of death associated with urban particle air pollution: a case-crossover analysis. Am J Epidemiol 2000; 151: 50–56. Zanobetti A, Bind MA, Schwartz J. Particulate air pollution and survival in a COPD cohort. Environ Health 2008; 7: 48. Andersen ZJ, Hvidberg M, Jensen SS, et al. Chronic obstructive pulmonary disease and long-term exposure to traffic-related air pollution: a cohort study. Am J Respir Crit Care Med 2011; 183: 455–461. Tsai SS, Chang CC, Yang CY. Fine particulate air pollution and hospital admissions for chronic obstructive pulmonary disease: a case-crossover study in Taipei. Int J Environ Res Public Health 2013; 10: 6015–6026. Gan WQ, FitzGerald JM, Carlsten C, et al. Associations of ambient air pollution with chronic obstructive pulmonary disease hospitalization and mortality. Am J Respir Crit Care Med 2013; 187: 721–727. Faustini A, Stafoggia M, Cappai G, et al. Short-term effects of air pollution in a cohort of patients with chronic obstructive pulmonary disease. Epidemiology 2012; 23: 861–879. Atkinson RW, Anderson HR, Sunyer J, et al. Acute effects of particulate air pollution on respiratory admissions: results from APHEA 2 project. Air Pollution and Health: a European Approach. Am J Respir Crit Care Med 2001; 164: 1860–1866. Halonen JI, Lanki T, Yli-Tuomi T, et al. Urban air pollution, and asthma and COPD hospital emergency room visits. Thorax 2008; 63: 635–641. Santus P, Russo A, Madonini E, et al. How air pollution influences clinical management of respiratory diseases. A case-crossover study in Milan. Respir Res 2012; 13: 95. Cirera L, Garcia-Marcos L, Gimenez J, et al. Daily effects of air pollutants and pollen types on asthma and COPD hospital emergency visits in the industrial and Mediterranean Spanish city of Cartagena. Allergol Immunopathol 2012; 40: 231–237. Faustini A, Stafoggia M, Colais P, et al. Air pollution and multiple acute respiratory outcomes. Eur Respir J 2013; 42: 304–313. de Hartog JJ, Ayres JG, Karakatsani A, et al. Lung function and indicators of exposure to indoor and outdoor particulate matter among asthma and COPD patients. Occup Environ Med 2010; 67: 2–10. Lagorio S, Forastiere F, Pistelli R, et al. Air pollution and lung function among susceptible adult subjects: a panel study. Environ Health 2006; 5: 11. Trenga CA, Sullivan JH, Schildcrout JS, et al. Effect of particulate air pollution on lung function in adult and pediatric subjects in a Seattle panel study. Chest 2006; 129: 1614–1622. Brauer M, Ebelt ST, Fisher TV, et al. Exposure of chronic obstructive pulmonary disease patients to particles: respiratory and cardiovascular health effects. J Expo Anal Environ Epidemiol 2001; 11: 490–500. Harre ES, Price PD, Ayrey RB, et al. Respiratory effects of air pollution in chronic obstructive pulmonary disease: a three month prospective study. Thorax 1997; 52: 1040–1044. Pope CA III, Kanner RE. Acute effects of PM10 pollution on pulmonary function of smokers with mild to moderate chronic obstructive pulmonary disease. Am Rev Respir Dis 1993; 147: 1336–1340. Hansel NN, McCormack MC, Belli AJ, et al. In-home air pollution is linked to respiratory morbidity in former smokers with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2013; 187: 1085–1090. Rice MB, Ljungman PL, Wilker EH, et al. Short-term exposure to air pollution and lung function in the Framingham Heart Study. Am J Respir Crit Care Med 2013; 188: 1351–1357. Forbes LJ, Kapetanakis V, Rudnicka AR, et al. Chronic exposure to outdoor air pollution and lung function in adults. Thorax 2009; 64: 657–663.
DOI: 10.1183/09031936.00108814
COPD AND ENVIRONMENT | E. GARSHICK
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DOI: 10.1183/09031936.00108814
Ackermann-Liebrich U, Leuenberger P, Schwartz J, et al. Lung function and long term exposure to air pollutants in Switzerland. Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) Team. Am J Respir Crit Care Med 1997; 155: 122–129. Schikowski T, Sugiri D, Ranft U, et al. Long-term air pollution exposure and living close to busy roads are associated with COPD in women. Respir Res 2005; 6: 152. Abbey DE, Burchette RJ, Knutsen SF, et al. Long-term particulate and other air pollutants and lung function in nonsmokers. Am J Respir Crit Care Med 1998; 158: 289–298. Churg A, Brauer M, del CA-C, et al. Chronic exposure to high levels of particulate air pollution and small airway remodeling. Environ Health Perspect 2003; 111: 714–718. Dai J, Xie C, Vincent R, et al. Air pollution particles produce airway wall remodeling in rat tracheal explants. Am J Respir Cell Mol Biol 2003; 29: 352–358. Schikowski T, Adam M, Marcon A, et al. Association of ambient air pollution with the prevalence and incidence of COPD. Eur Respir J 2014; 44: 614–626. Downs SH, Schindler C, Liu LJ, et al. Reduced exposure to PM10 and attenuated age-related decline in lung function. N Engl J Med 2007; 357: 2338–2347. Hardin M, Silverman EK, Barr RG, et al. The clinical features of the overlap between COPD and asthma. Respir Res 2011; 12: 127. Calverley PM, Burge PS, Spencer S, et al. Bronchodilator reversibility testing in chronic obstructive pulmonary disease. Thorax 2003; 58: 659–664. Vonk JM, Jongepier H, Panhuysen CI, et al. Risk factors associated with the presence of irreversible airflow limitation and reduced transfer coefficient in patients with asthma after 26 years of follow up. Thorax 2003; 58: 322–327. Dadvand P, Nieuwenhuijsen MJ, Agusti A, et al. Air pollution and biomarkers of systemic inflammation and tissue repair in COPD patients. Eur Respir J 2014; 44: 603–613. Dubowsky SD, Suh H, Schwartz J, et al. Diabetes, obesity, and hypertension may enhance associations between air pollution and markers of systemic inflammation. Environ Health Perspect 2006; 114: 992–998. Hoffmann B, Moebus S, Dragano N, et al. Chronic residential exposure to particulate matter air pollution and systemic inflammatory markers. Environ Health Perspect 2009; 117: 1302–1308. Delfino RJ, Staimer N, Tjoa T, et al. Circulating biomarkers of inflammation, antioxidant activity, and platelet activation are associated with primary combustion aerosols in subjects with coronary artery disease. Environ Health Perspect 2008; 116: 898–906. Sullivan JH, Hubbard R, Liu SL, et al. A community study of the effect of particulate matter on blood measures of inflammation and thrombosis in an elderly population. Environ Health 2007; 6: 3. Steinvil A, Kordova-Biezuner L, Shapira I, et al. Short-term exposure to air pollution and inflammation-sensitive biomarkers. Environ Res 2008; 106: 51–61. Williams LA, Ulrich CM, Larson T, et al. Proximity to traffic, inflammation, and immune function among women in the Seattle, Washington, area. Environ Health Perspect 2009; 117: 373–378. Forbes LJ, Patel MD, Rudnicka AR, et al. Chronic exposure to outdoor air pollution and markers of systemic inflammation. Epidemiology 2009; 20: 245–253. Gan WQ, Man SF, Senthilselvan A, et al. Association between chronic obstructive pulmonary disease and systemic inflammation: a systematic review and a meta-analysis. Thorax 2004; 59: 574–580.
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Effects of short- and long-term exposures to ambient air pollution on COPD Eric Garshick Affiliations: Pulmonary and Critical Care Medicine Section, Medical Service, VA Boston Healthcare System, Channing Division of Network Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA. Correspondence: Eric Garshick, Pulmonary and Critical Care Medicine Section, VA Boston Healthcare System, 1400 VFW Parkway, West Roxbury, MA 02132, USA. E-mail: [email protected]
@ERSpublications Two papers in the current issue of ERJ address the link between air pollution exposure and COPD http://ow.ly/yEq23 The London fog episode in 1952 was a sentinel event that indicated that short-term exposure to ambient air pollution could adversely influence the health of persons with chronic obstructive pulmonary disease (COPD). A review of autopsy records indicated a doubling of cases with COPD as a major finding compared with other periods [1]. The association between greater levels of ambient air pollution measured in the community and an increase in subsequent short-term COPD-related mortality and hospitalisations has been confirmed by analysis of health related administrative data, including records of hospital admissions and emergency room visits in the USA, Asia and Europe [2–14]. There are considerably fewer studies assessing the impact of short-term air pollution exposure in COPD patients with disease documented by spirometry. Overall, these studies suggest that COPD patients experience a reduction in pulmonary function as a result of short-term exposures [15–20]. Remarkably, the majority of these previous studies included relatively few subjects and with one exception [21] were not designed to assess exacerbation risk. The study that assessed exacerbation risk [21] included former smokers with moderate-to-severe COPD and measured indoor levels of particles with a cut-off aerodynamic diameter of 2.5 mm (PM2.5) and NO2. Higher levels were significantly associated with more symptoms and an increased risk of experiencing an exacerbation, suggesting that measurement of indoor levels of pollutants in persons who spend considerable time indoors (such as those with significant COPD) may be a more relevant measure of exposure than outdoor levels more commonly assessed. The most robust assessment of the effects of ambient air pollution on pulmonary function (but not limited to patients with COPD) included 3262 former and never smokers (some with repeated assessment) from the US Framingham Heart Study in which spirometry data obtained in 1995–2011 were linked to central-site PM2.5, ozone and NO2 [22]. Pollution measured 24–48 h before spirometry and within ranges considered ‘‘moderate’’ by the US Environmental Protection Agency was associated with a significant reduction in forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC). Mean FEV1 and FVC were normal but 20% were defined as having either asthma or COPD based on physician diagnosis, medication use or symptoms. The effects of pollution were not greater in persons with asthma or COPD. The question of whether chronic air pollution exposure can result in the development of COPD is less clear. Previous cross-sectional studies conducted have suggested an association between long-term air pollution exposure, reduced pulmonary function and increased risk of COPD [23–26]. Two large prospective population-based studies from Denmark [6] and metropolitan Vancouver (BC, Canada) [8] did not have Received: June 14 2014
|
Accepted: June 16 2014
Support statement: E. Garshick has received grants from the National Institute of Environmental Health Sciences (R01 ES019853). Conflict of interest: None declared. Copyright ßERS 2014
558
Eur Respir J 2014; 44: 558–561 | DOI: 10.1183/09031936.00108814
COPD AND ENVIRONMENT | E. GARSHICK
access to pulmonary function data and defined new-onset COPD based on hospitalisation records. Significant associations between a first COPD hospitalisation and modelled NO2 [6], and particulate air pollution as measured by black carbon [8] were observed. Further support of a causal relationship is evidence that chronic particulate air pollution exposure results small airway wall remodelling. In a comparison of lungs obtained at autopsy from non-smoking Mexico City (Mexico) residents (high pollution) and Vancouver residents (low pollution) without previous lung disease, small airways had increased amounts of muscle and fibrous tissue, consistent with remodelling [27]. In a rat model, urban air particles also induced the expression of genes involved in airway wall fibrosis [28]. SCHIKOWSKI et al. [29] assess the impact of pollution on the incidence and prevalence of COPD in a longitudinal study in this issue of the European Respiratory Journal. To obtain a large sample size and achieve a common approach to exposure assessment, they analysed subjects who had previously participated in one of four previous European air pollution studies, had pulmonary function assessed longitudinally with two tests available and who lived in areas where the European Study of Cohorts for Air Pollution Effects (ESCAPE) project modelled residential exposure to PM (n53692) and NO2 (n56550) in 2008–2011. COPD was defined based on the NHANES (National Health and Nutrition Examination Survey) defined lower limits of normal for FEV1/FVC (which provided results similar to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) cut-off value of FEV1/FVC ,0.70). Based on data collected in 2008–2011, exposure model derived values included PM2.5, PM10, NO2, oxides of nitrogen (NOx) and measures of traffic volume. NO2 and PM10 were extrapolated retrospectively using historical air pollution records to provide estimates for the follow-up time-point in all studies and the baseline test in three studies, but it was not possible to extrapolate the traffic data. Although not precisely stated, follow-up of the four cohorts ranged from approximately 11 to 15 years, starting in 1985–1999 with follow-up through 2001–2012. The authors used logistic regression to assess the association between COPD prevalence and incidence defined at follow-up by spirometrically defined cut-offs and air pollution exposures defined using the 2008–2011 exposure model linked to home address. Study specific effect estimates were combined in a meta-analysis, and overall effect estimates (other than for coarse PM) were generally positive but not significantly associated with COPD, other than with measures of traffic volume in females and in neversmokers. Results were similar (but weaker) when extrapolated exposures for NO2 and PM10 were used. The authors appropriately note that due to the many non-statistically significant associations reported, it was not possible to determine whether ambient air pollution contributed to the development of COPD. As the authors note, uncertainty in exposure assessment would make it more difficult to detect associations. An acknowledged limitation is the lack of concurrent exposure measurements and details regarding the extent that the address used to assign exposure in each of the analyses remained stable over the follow-up period are not provided. However, there are also other significant limitations. COPD, as defined by the investigators, was relatively uncommon in most of the study population. At follow-up, the mean ages of European Community Respiratory Health Survey and National Survey of Health and Development populations, which together accounted for more than half the study cohort, were only 43 and 53 years old, respectively. Accordingly, these studies contributed relatively few cases since COPD is primarily a disease of older individuals. Part of the Swiss study on Air Pollution and Lung Disease in adults (SAPALDIA) cohort was included in the population analysed by SCHIKOWSKI et al. [29]. A previous analysis of the effect of particulate air pollution in the full SAPALDIA cohort [30] did not define the outcome categorically, but used pulmonary function as a continuous outcome measure, and reported an improvement in FEV1 as PM10 decreased. A similar approach in the current study would likely have increased the power of the study to detect an effect of exposure. This would be an appropriate approach since a subclinical decline in pulmonary function precedes the development of more significant disease defined using a discrete pulmonary function cut point. Finally, persons who reported asthma either at baseline or follow-up were excluded from analysis. This might be appropriate in a younger population since it would be unlikely that these persons would have true COPD at baseline. However, in persons who subsequently develop disease and in the older individuals in the study population there is likely to be overlap with persons meeting diagnostic criteria for COPD since clinical characteristics of asthma and COPD may overlap [31–33]. A sensitivity analysis that included subjects with presumed asthma might provide additional insight. In a second paper in this issue of European Respiratory Journal, DADVAND et al. [34] report on the effects of exposure to NO2 and PM2.5 on inflammatory biomarkers using land-use regression models developed by ESCAPE in 242 patients with well-documented COPD in metropolitan Barcelona in 2004–2006. Although positive associations between air pollution and elevated circulating inflammatory markers have been reported in previous studies including persons without COPD [35–37], such reports have not been consistently positive [38–41]. Since COPD is already characterised by systemic and pulmonary inflammation [42], it is possible that COPD patients may be particularly sensitive to effects of air pollution on promoting systemic inflammation. DADVAND et al. [34] noted positive associations between
DOI: 10.1183/09031936.00108814
559
COPD AND ENVIRONMENT | E. GARSHICK
short-term exposures (5-day lag) to NO2 and an increase in C-reactive protein and fibrinogen, with a suggestive association with other inflammatory biomarkers and a greater effect in former smokers. There was considerably less evidence for an effect of long-term (.1 year) exposures on these biomarkers. The authors did not provide insight into the lack of association with PM2.5 with these biomarkers that they observed. Exposure to ambient NO2 is a measure of exposure to vehicle exhaust, but one would expect PM2.5 levels to reflect these exposures in an urban environment since vehicular sources also contribute to particulate air pollution. The reasons for lack of an association are uncertain, but likely reflect imprecision in modelling daily exposures. Daily exposure in 2004–2006 was extrapolated from 2009 address-specific annual averages obtained from the land-use regression model. Temporal variability was estimated based on variation of daily background in 2004–2006 obtained from local NO2 and PM10 monitors, and the PM10 data were subsequently used to estimate temporal changes in PM2.5. To summarise, although the findings of both papers are limited by imprecision in exposure assessment, the paper by SCHIKOWSKI et al. [29] is consistent with previous literature suggesting that long-term exposure to air pollution may result in the development COPD. The paper by DADVAND et al. [34] is consistent with the effects of recent air pollution exposures on promoting systemic inflammation. Efforts at improving the precision of exposure estimates in the design of future studies will improve the ability to detect meaningful associations between air pollution exposures and COPD risk, and the effects of air pollution on promoting systemic inflammation in patients with COPD.
References 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23
560
Hunt A, Abraham JL, Judson B, et al. Toxicologic and epidemiologic clues from the characterization of the 1952 London smog fine particulate matter in archival autopsy lung tissues. Environ Health Perspect 2003; 111: 1209–1214. Dominici F, Peng RD, Bell ML, et al. Fine particulate air pollution and hospital admission for cardiovascular and respiratory diseases. JAMA 2006; 295: 1127–1134. Atkinson RW, Kang S, Anderson HR, et al. Epidemiological time series studies of PM2.5 and daily mortality and hospital admissions: a systematic review and meta-analysis. Thorax 2014; 69: 660–665. Sunyer J, Schwartz J, Tobias A, et al. Patients with chronic obstructive pulmonary disease are at increased risk of death associated with urban particle air pollution: a case-crossover analysis. Am J Epidemiol 2000; 151: 50–56. Zanobetti A, Bind MA, Schwartz J. Particulate air pollution and survival in a COPD cohort. Environ Health 2008; 7: 48. Andersen ZJ, Hvidberg M, Jensen SS, et al. Chronic obstructive pulmonary disease and long-term exposure to traffic-related air pollution: a cohort study. Am J Respir Crit Care Med 2011; 183: 455–461. Tsai SS, Chang CC, Yang CY. Fine particulate air pollution and hospital admissions for chronic obstructive pulmonary disease: a case-crossover study in Taipei. Int J Environ Res Public Health 2013; 10: 6015–6026. Gan WQ, FitzGerald JM, Carlsten C, et al. Associations of ambient air pollution with chronic obstructive pulmonary disease hospitalization and mortality. Am J Respir Crit Care Med 2013; 187: 721–727. Faustini A, Stafoggia M, Cappai G, et al. Short-term effects of air pollution in a cohort of patients with chronic obstructive pulmonary disease. Epidemiology 2012; 23: 861–879. Atkinson RW, Anderson HR, Sunyer J, et al. Acute effects of particulate air pollution on respiratory admissions: results from APHEA 2 project. Air Pollution and Health: a European Approach. Am J Respir Crit Care Med 2001; 164: 1860–1866. Halonen JI, Lanki T, Yli-Tuomi T, et al. Urban air pollution, and asthma and COPD hospital emergency room visits. Thorax 2008; 63: 635–641. Santus P, Russo A, Madonini E, et al. How air pollution influences clinical management of respiratory diseases. A case-crossover study in Milan. Respir Res 2012; 13: 95. Cirera L, Garcia-Marcos L, Gimenez J, et al. Daily effects of air pollutants and pollen types on asthma and COPD hospital emergency visits in the industrial and Mediterranean Spanish city of Cartagena. Allergol Immunopathol 2012; 40: 231–237. Faustini A, Stafoggia M, Colais P, et al. Air pollution and multiple acute respiratory outcomes. Eur Respir J 2013; 42: 304–313. de Hartog JJ, Ayres JG, Karakatsani A, et al. Lung function and indicators of exposure to indoor and outdoor particulate matter among asthma and COPD patients. Occup Environ Med 2010; 67: 2–10. Lagorio S, Forastiere F, Pistelli R, et al. Air pollution and lung function among susceptible adult subjects: a panel study. Environ Health 2006; 5: 11. Trenga CA, Sullivan JH, Schildcrout JS, et al. Effect of particulate air pollution on lung function in adult and pediatric subjects in a Seattle panel study. Chest 2006; 129: 1614–1622. Brauer M, Ebelt ST, Fisher TV, et al. Exposure of chronic obstructive pulmonary disease patients to particles: respiratory and cardiovascular health effects. J Expo Anal Environ Epidemiol 2001; 11: 490–500. Harre ES, Price PD, Ayrey RB, et al. Respiratory effects of air pollution in chronic obstructive pulmonary disease: a three month prospective study. Thorax 1997; 52: 1040–1044. Pope CA III, Kanner RE. Acute effects of PM10 pollution on pulmonary function of smokers with mild to moderate chronic obstructive pulmonary disease. Am Rev Respir Dis 1993; 147: 1336–1340. Hansel NN, McCormack MC, Belli AJ, et al. In-home air pollution is linked to respiratory morbidity in former smokers with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2013; 187: 1085–1090. Rice MB, Ljungman PL, Wilker EH, et al. Short-term exposure to air pollution and lung function in the Framingham Heart Study. Am J Respir Crit Care Med 2013; 188: 1351–1357. Forbes LJ, Kapetanakis V, Rudnicka AR, et al. Chronic exposure to outdoor air pollution and lung function in adults. Thorax 2009; 64: 657–663.
DOI: 10.1183/09031936.00108814
COPD AND ENVIRONMENT | E. GARSHICK
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DOI: 10.1183/09031936.00108814
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